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Fig. 1. Cardiac morphogenesis in different genetic backgrounds. (A)
Depiction of several key stages of zebrafish heart formation, beginning with
the juxtaposition of two bilateral cardiac progenitor cell populations along
the midline of the embryo (dotted line) to the elongation of the heart tube
along the anterior-posterior axis. Dorsal view onto heart field. See text for
detailed explanations. (B-I) cmlc2, (J,K) vmhc and (L,M)
amhc expression. Embryos are 30-32 hpf. Parts L and M were captured
with a 30° angle from dorsal for better visualization of atrial
morphology. (B-D) Comparison of wild-type, has/prkci morphant
and Tg(cmlc2:prkci) transgenic and has/prkci
morphant embryos. (E) Heart cone formation is not completed, resulting
in bilateral wings of myocardial progenitor cells (arrowheads) in
prkci2A kinase-dead mutants. (F,G) Heart cone
`tilting' occurs, but heart tube elongation is delayed to varying degrees in
nok mutants. (F) Severe and (G) medium-strength phenotypes.
(H) nok/mpp5 morphants display a severe heart tube elongation
defect. (I) Co-injection of nok/mpp5 MO with wild-type
nok/mpp5 mRNA rescues myocardial morphogenesis. There is no
developmental delay. (J,K) Length of the ventricle is affected in
nok mutants. (L,M) Length of the atrium is shortened and,
along the mediolateral axis, narrower than wild type. (N,O)
noks305 mutants and embryos that express high levels of
PRKCi2A mutant protein (overexpression phenotype) are
phenotypically similar. The body axis is curved ventrally and the retinal
pigmented epithelium is largely disrupted, leaving the central portion of the
retina uncovered, a phenotype more severe than in has mutants.
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